NF-κB介导的炎性反应在HIV/AIDS肺脾气虚证中的机制研究
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摘要
HIV/AIDS是由HIV引起的患者免疫系统进行性损伤的免疫缺陷性疾病,炎性反应在HIV/AIDS的疾病发展进程中起重要作用。NF-κB是引起炎性反应的关键转录因子,可调节多种基因的表达,因此,NF-κB介导的炎性反应是HIV/AIDS患者的疾病发展的机制之一。系统生物学研究发现,HIV/AIDS不同中医证候患者有不同的分子物质基础,在HIV/AIDS肺脾气虚证患者的转录组学检测中发现,有与NF-κB介导的炎性反应相关的基因异常表达,可能与HIV/AIDS肺脾气虚证的疾病发展有一定关系,探讨NF-κB介导的炎性反应在HIV/AIDS肺脾气虚证中的研究现状,为下一步HIV/AIDS肺脾气虚证的机制研究提供新的研究点,为中医药治疗HIV/AIDS的研究提供新的靶点。
HIV/AIDS is an immunodeficiency disease caused by human immunodeficiency virus(HIV), and the inflammatory response plays an important role in the development of HIV/AIDS. NF-κB is a key transcription factor that causes inflammation and regulates the expression of multiple genes. Therefore, the inflammatory response mediated by NF-κB is one of the mechanisms for the disease development of HIV/AIDS. Systems biology studies have found that HIV/AIDS patients with different syndromes have different molecular material foundation. The transcriptome study found that the NF-κB mediated gene abnormal expression associated with the inflammatory response. It may be related to HIV/AIDS disease. Exploring the NF-κB mediated inflammatory response in HIV/AIDS research status in HIV/AIDS patients with lung and spleen qi deficiency syndrome to provide a new research point for the next step of mechanism research of HIV/AIDS with lung and spleen qi deficiency syndrome and a new target for research on the treatment of HIV/AIDS with traditional Chinese medicine.
HIV/AIDS is an immunodeficiency disease caused by human immunodeficiency virus(HIV), and the inflammatory response plays an important role in the development of HIV/AIDS. NF-κB is a key transcription factor that causes inflammation and regulates the expression of multiple genes. Therefore, the inflammatory response mediated by NF-κB is one of the mechanisms for the disease development of HIV/AIDS. Systems biology studies have found that HIV/AIDS patients with different syndromes have different molecular material foundation. The transcriptome study found that the NF-κB mediated gene abnormal expression associated with the inflammatory response. It may be related to HIV/AIDS disease. Exploring the NF-κB mediated inflammatory response in HIV/AIDS research status in HIV/AIDS patients with lung and spleen qi deficiency syndrome to provide a new research point for the next step of mechanism research of HIV/AIDS with lung and spleen qi deficiency syndrome and a new target for research on the treatment of HIV/AIDS with traditional Chinese medicine.
引文
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[25]Mcginty T,Mirmonsef P,Mallon D P,et al.Does systemic inflammation and immune activation contribute to fracture risk in HIV?.Current Opinion in Hiv&Aids,2016,11(3):253-260
[26]Natsag J,Kendall M,Sellmeyer D,et al.Vitamin D,osteoprotegerin/receptor activator of nuclear factor-kappa B ligand(OPG/RANKL)and inflammation with alendronate treatment in HIV-infected patients with reduced bone mineral density.Hiv Medicine,2016,17(3):196-205
[27]Nitkiewicz J,Borjabad A,Morgello S,et al.HIV induces expression of complement component C3 in astrocytes by NF-κB-dependent activation of interleukin-6 synthesis.Journal of Neuroinflammation,2017,14(1):23
[28]Jesús S M,ángeles M F M,álvarez Susana.HIV-1 increases TLR responses in human primary astrocytes.Scientific Reports,2015,5(4):17887
[29]Zhang G,Liu R,Zhong Y,et al.Down-regulation of NF-κB transcriptional activity in HIV-associated kidney disease by BRD4 inhibition.Journal of Biological Chemistry,2012,287(34):28840-28851
[30]徐立然,王东旭,郭建中,等.HIV感染无症状期患者中医证型分布规律研究.中国中西医结合杂志,2013,331(7):896-900
[31]谢世平,陈建设,刘爱华,等.艾滋病常见虚证量化诊断的Logistic回归分析.中华中医药杂志,2010,25(10):1663-1665
[32]王健,刘颖,何丽云,等.2 237例HIV/AIDS患者中医证候分布及演变规律.中医杂志,2012,53(11):948-951
[33]谢世平,张淼,张海燕,等.运用系统生物学“组学”技术研究HIV/AIDS中医证候的思路与方法.哈尔滨:中华中医药学会防治艾滋病分会,2014:12
[34]Liu S,Chen Y,Xie S,et al.Gene expression profiles of HIV/AIDS patients with Qi-Yin Deficiency and Dampness-Heat Retention.Journal of Alternative&Complementary Medicine,2016,22(11):865-879
[2]Gonzalez S M,Taborda N A,Correa L A,et al.Particular activation phenotype of T cells expressing HLA-DR but not CD38 in GALT from HIV-controllers is associated with immune regulation and delayed progression to AIDS.Immunologic Research,2016,64(3):765-774
[3]Bhargavan B,Woollard S M,Kanmogne G D.Toll-like receptor-3mediates HIV-1 transactivation via NFκB and JNK pathways and histone acetylation,but prolonged activation suppresses Tat and HIV-1 replication.Cellular Signalling,2016,28(2):7
[4]谢世平,侯明杰,祝应俊,等.艾滋病中医基本证候专家问卷调查分析.中国中医基础医学杂志,2009,15(1):56-58
[5]Sarnico I,Lanzillotta A,Benarese M,et al.NF-kappaB dimers in the regulation of neuronal survival.International Review of Neurobiology,2009,85(85):351
[6]吴亚楠,赵鹏翔,马雪梅.NF-κB研究进展及其与炎症的关系.安徽农业科学,2012,40(34):16533-16535
[7]Zhang Z,Rigas B.NF-kappaB,inflammation and pancreatic carcinogenesis:NF-kappa B as a chemoprevention target(review).International Journal of Oncology,2006,29(1):185
[8]Kaileh M,Sen R.Role of NF-kappaB in the anti-inflammatory effects of tocotrienols.Journal of the American College of Nutrition,2010,29(sup3):S334-S339
[9]H?cker H,Karin M.Regulation and function of IKK and IKKrelated kinases.Sciences Stke Signal Transduction Knowledge Environment,2006,2006(357):re13
[10]楼希文,孙绍刚,王琛.转录因子NF-кB的核内活性调控.中国细胞生物学学报,2009,31(6):741-748
[11]Lang A,Schoonhoven R,Tuvia S,et al.Nuclear factor-κB in proliferation,activation,and apoptosis in rat hepatic stellate cells.J Hepatol,2000,33(1):49-58
[12]Potoka D A,Nadler E P,Zhou X,et al.Inhibition of NF-kappa B by Ikappa B prevents cytokine-induced NO production and promotes enterocyte apoptosis in vitro.Shock,2000,14(3):366-373
[13]Xiao Y,Liang L,Huang M,et al.Bromodomain and extra-terminal domain bromodomain inhibition prevents synovial inflammation via blocking IκB kinase:Dependent NF-κB activation in rheumatoid fibroblast-like synoviocytes.Rheumatology,2016,55(1):173
[14]Rubioperez J M,Morillasruiz J M.A review:Inflammatory process in Alzheimer’s disease,role of cytokines.The Scientific World Journal,2012,2012(6):756357
[15]Sampey G C,Saifuddin M,Schwab A,et al.Exosomes from HIV-1-infected cells stimulate production of pro-inflammatory cytokines through trans-activating response(TAR)RNA.Journal of Biological Chemistry,2016,291(3):1251
[16]Mamik M K,Banerjee S,Walseth T F,et al.HIV-1 and IL-1βregulate astrocytic CD38 through mitogen-activated protein kinases and nuclear factor-κB signaling mechanisms.Journal of Neuroinflammation,2011,8(1):1-13
[17]Feng T,Gan J,Qin A,et al.HIV 1 downregulates the expression and phosphorylation of receptor tyrosine kinase by targeting the NF-κB pathway.Molecular Medicine Reports,2016,14(3):1947
[18]Ivanova A,Shilpi R Y,Sachdeva R,et al.Native X-DING-CD4protein secreted by HIV-1 resistant CD4+T cells blocks activity of IL-8 promoter in human endothelial cells infected with enteric bacteria.Innate Immunity,2012,18(4):571
[19]Equils O,Schito M L,Karahashi H,et al.Toll-like receptor 2(TLR2)and TLR9 signaling results in HIV-long terminal repeat transactivation and HIV replication in HIV-1 transgenic mouse spleen cells:implications of simultaneous activation of TLRs on HIV replication.J Immunol,2003,170(10):5159-5164
[20]Roesch F,Richard L,Rua R,et al.Vpr enhances tumor necrosis factor production by HIV-1-infected T cells.Journal of Virology,2015,89(23):12118-12130
[21]Ben H N,Planès R,Leghmari K,et al.HIV-1 Tat protein induces production of proinflammatory cytokines by human dendritic cells and monocytes/macrophages through engagement of TLR4-MD2-CD14 complex and activation of NF-κB pathway.Plos One,2015,10(6):e0129425
[22]Fiume G,Scialdone A,Albano F,et al.Impairment of T cell development and acute inflammatory response in HIV-1 Tat transgenic mice.Scientific Reports,2015,5(13864):13864
[23]Soo Y G,Ju S M,Choi S Y,et al.HDAC6 mediates HIV-1 tat-induced proinflammatory responses by regulating MAPK-NF-kappa B/AP-1pathways in astrocytes.Glia,2015,63(11):1953-1965
[24]Youn G S,Kwon D J,Ju S M,et al.Celastrol ameliorates HIV-1Tat-induced inflammatory responses via NF-kappa B and AP-1inhibition and heme oxygenase-1 induction in astrocytes.Toxicology&Applied Pharmacology,2014,280(1):42-52
[25]Mcginty T,Mirmonsef P,Mallon D P,et al.Does systemic inflammation and immune activation contribute to fracture risk in HIV?.Current Opinion in Hiv&Aids,2016,11(3):253-260
[26]Natsag J,Kendall M,Sellmeyer D,et al.Vitamin D,osteoprotegerin/receptor activator of nuclear factor-kappa B ligand(OPG/RANKL)and inflammation with alendronate treatment in HIV-infected patients with reduced bone mineral density.Hiv Medicine,2016,17(3):196-205
[27]Nitkiewicz J,Borjabad A,Morgello S,et al.HIV induces expression of complement component C3 in astrocytes by NF-κB-dependent activation of interleukin-6 synthesis.Journal of Neuroinflammation,2017,14(1):23
[28]Jesús S M,ángeles M F M,álvarez Susana.HIV-1 increases TLR responses in human primary astrocytes.Scientific Reports,2015,5(4):17887
[29]Zhang G,Liu R,Zhong Y,et al.Down-regulation of NF-κB transcriptional activity in HIV-associated kidney disease by BRD4 inhibition.Journal of Biological Chemistry,2012,287(34):28840-28851
[30]徐立然,王东旭,郭建中,等.HIV感染无症状期患者中医证型分布规律研究.中国中西医结合杂志,2013,331(7):896-900
[31]谢世平,陈建设,刘爱华,等.艾滋病常见虚证量化诊断的Logistic回归分析.中华中医药杂志,2010,25(10):1663-1665
[32]王健,刘颖,何丽云,等.2 237例HIV/AIDS患者中医证候分布及演变规律.中医杂志,2012,53(11):948-951
[33]谢世平,张淼,张海燕,等.运用系统生物学“组学”技术研究HIV/AIDS中医证候的思路与方法.哈尔滨:中华中医药学会防治艾滋病分会,2014:12
[34]Liu S,Chen Y,Xie S,et al.Gene expression profiles of HIV/AIDS patients with Qi-Yin Deficiency and Dampness-Heat Retention.Journal of Alternative&Complementary Medicine,2016,22(11):865-879